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TRANSTHYRETIN (PREALBUMIN) GENE IN HUMAN PRIMARY HEPATIC CANCER

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Science China Chemistry 1991年第11期34卷 1312-1318页

作者：顾建人蒋惠秋贺丽萍李岱宗周筱梅戴卫列钱莲芳陈渊卿 C. SCHWEINFEST T. PAPAS notional laboratory for oncogenes and related genes Shanghai Cancer InstituteShanghai 200032 PRC laboratory of Molecular Oncology National Cancer Institute(NCI-FCRDC)USA

From a subtracting cDNA library constructed from normal liver versus human primary hepatic cancer (PHC), a cDNA clone pG8 was isolated. Using it as a probe, RNA extracted from one human liver and 9 PHC samples were analyzed by Northern hybridization. As expected, its mRNA was highly expressed in liver; however, the expression was strikingly suppressed in PHC. Only weak signal was observed in 2 out of 9 PHC, while no signal was detectable in the other 7 samples. Utilizing pG8 as a probe, DNA from the same PHC specimens was analyzed after MspI digestion and Southern hybridization. Deletion of DNA fragment was observed in 4 out of 9 samples. In further study of cancer and non-cancerous liver from other 7 PHC patients, similar deletion of DNA fragments in cancer was observed in 4 out of 7 samples. After sequencing of the clone of 572 bp, it was unexpectedly found that pG8 was completely homologous to the coding sequence of transthyretin, TTR gene, as TTR (or prealbumin) gene has been known to be linked to a hereditary disorder, familial amyloidosis (FAP), and related to thyroxine transport and binding to retinol-RBP (the retinol binding protein) complex. This is the first report of a study on TTR in human primary hepatic cancer. Since TTR gene was strikingly suppressed in mRNA expression and possibly defective in its gene structure, it was strongly implicated that TTR might be an important gene marker or a candidate of anti-oncogene for human PHC. The biological activity of TTR gene is under study.

关键词： hepatoma subtracting cDNA library suppression deletion.

Cloning and characterization of human IC53-2, a novel CDK5 activator binding protein

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Cell Research 2003年第2期13卷 83-91页

作者： YI Hu XIE, XIANG Huo HE, YUN TIAN TANG, JIN JUN LI, Zm MEI PAN, WEN XIN QIN, DA FANG WAN , JIAN REN GU,1 State Key laboratory of oncogenes and related genes, Shanghai Cancer Institute, Shanghai 200032, China 2Peopele’s Hospital of Guangxi Zhuang Autonomous Region, Nanning 530021, China 1State Key laboratory of oncogenes and related genes Shanghai Cancer Institute Shanghai 200032 China 1State Key laboratory of oncogenes and related genes Shanghai Cancer Institute Shanghai 200032 China 2Peopele s Hospital of Guangxi Zhuang Autonomous Region Nanning 530021 China 1State Key laboratory of oncogenes and related genes Shanghai Cancer Institute Shanghai 200032 China 1State Key laboratory of oncogenes and related genes Shanghai Cancer Institute Shanghai 200032 China 1State Key laboratory of oncogenes and related genes Shanghai Cancer Institute Shanghai 200032 China 1State Key laboratory of oncogenes and related genes Shanghai Cancer Institute Shanghai 200032 China 1State Key laboratory of oncogenes and related genes Shanghai Cancer Institute Shanghai 200032 China

We have identified IC53-2, a human homologue of the rat C53 gene from a human placenta cDNA library (GeneBank Accession ***217982). IC53-2 can bind to the CDK5 activator p35 by in vitro association assay. IC53-2 is mapped to human chromosome 17q21.31. The IC53-2 transcript is highly expressed in kidney, liver, skeletal muscle and placenta. It is abundantly expressed in SMMC-7721, C-33A, 3AO, A431 and MCF-7 cancer cell lines by RT-PCR assay. Stable transfection of IC53-2 cDNA into the hepatocellular carcinoma SMMC-7721 cell remarkably stimulates its growth in vitro. The above results indicate that IC53-2 is a novel human gene, which may be involved in the regulation of cell proliferation.

关键词： IC53-2 CDK5 p35 hepatocellular carcinoma proliferation.

A novel gene delivery system targeting cells expressing VEGF receptors

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Cell Research 1999年第1期9卷 11-25页

作者： LI JUN MIN JUN SONG HAN YI HUANG PEI KUN TIAN SHU MIN QU MIN YAO HUI QIU JIANG DA FANG WAN JING CHU LUO CHENG XIAO GU JIAN REN GU( National Labomtory for oncogenes and related genes, Shanghai Cancer Institute, Shanghai 200032,China)(National laboratory of 1National laboratory for oncogenes and related genes Shanghai Cancer Institute Shanghai 200032 China 1National laboratory for oncogenes and related genes Shanghai Cancer Institute Shanghai 200032 China 1National laboratory for oncogenes and related genes Shanghai Cancer Institute Shanghai 200032 China 1National laboratory for oncogenes and related genes Shanghai Cancer Institute Shanghai 200032 China 1National laboratory for oncogenes and related genes Shanghai Cancer Institute Shanghai 200032 China 1National laboratory for oncogenes and related genes Shanghai Cancer Institute Shanghai 200032 China 1National laboratory for oncogenes and related genes Shanghai Cancer Institute Shanghai 200032 China 1National laboratory for oncogenes and related genes Shanghai Cancer Institute Shanghai 200032 China 2National laboratory of Protein Engineering and Plant Genetic Engineering Peking University Beijing 100871 China 2National laboratory of Protein Engineering and Plant Genetic Engineering Peking University Beijing 100871 China 1National laboratory for oncogenes and related genes Shanghai Cancer Institute Shanghai 200032 China

Two ligand oligopeptides GV1 and GV2 were designed according to the putative binding region of VEGF to its receptors. GV1, GV2 and endosome releasing oligopeptide HA20 were conjugated with poly-L-lysine or protamine and the resulting conjugates could interact with DNA in a noncovalent bond to form a complex. Using pSV2-β-galactosidase as a reporter gene, it has been demonstrated that exogenous gene was transferred into bovine aortic arch-derived endothelial cells (ABAE) andhuman malignant melanoma cell lines (A375) in vitro. In vivo experiments, exogenous gene was transferred into tumor vascular endothelial cells and tumor cells of subcutaneously transplanted human colon cancer LOVO, human malignant melanoma A375 and human hepatoma graft in nude mice. This system could also target gene to intrahepatically transplanted human hepatoma injected via portal vein in nude mice. These results are correlated with theGene delivery system targeting VEGF receptors relevant receptors (flt-1, flk-1/KDR) expression on the targeted cells and tissues.

关键词： VEGF receptors gene delivery system tumor vascular endothelial cells targeting

Human chromosome pellicle antibody recognizing centromere protein-C(CENP-C),the main component of the kinetochore

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Cell Research 1997年第1期7卷 13-19页

作者： XIE YONG ZU MEI NI JIAN REN GU PHIL WONG WEN QING WU GUO WEI XU(Hong Kong University of Science and Technology,Department of Biology, Hong Kong) (Shanghai Institute of Cell Biology, Chinese Academy of Sciences, Shanghai) (Shanghai Cancer Institute, Nation Shanghai Cancer Institute National Laboratory for Oncogenes and Related Genes Shanghai

Recently the antichromosome antisera from several scleroderma patients have been found to recognize the pellicle of metaphase and anaphase chromosomes. In order to identify the pellicle components, we used these antichromosome antisera to screen a human embryonic cDNA library. The sequences of the positive clones are identical to the cDNA gene sequence of CENP-C (centromere protein C), a human centromere autoantigen. This result suggusts that CENP-C is a component of the pellicle of human metaphase and anaphase chromosomes.

关键词： Human antibody scleroderma CENP-C (centromere protein C) metaphase chromosome pellicle indirect immunofluorescent staining

Treatment of solid tumors with chimeric antigen receptor-engineered T cells: current status and future prospects

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Science China(Life Sciences) 2016年第4期59卷 360-369页

作者： Shengmeng Di Zonghai Li State Key laboratory of oncogenes & related genes Shanghai Cancer Institute Renji Hospital Shanghai Jiaotong University School of Medicine

Chimeric antigen receptors(CARs) are artificial recombinant receptors that generally combine the antigen-recognition domain of a monoclonal antibody with T cell activation domains. Recent years have seen great success in clinical trials employing CD19-specific CAR-T cell therapy for B cell leukemia. Nevertheless, solid tumors remain a major challenge for CAR-T cell therapy. This review summarizes the preclinical and clinical studies on the treatment of solid tumors with CAR-T cells. The major hurdles for the success of CAR-T and the novel strategies to address these hurdles have also been described and discussed.

关键词： solid tumor adoptive cell therapy T cell chimeric antigen receptor

Exploring the mechanism of Xiaoaiping Injection inhibiting autophagy in prostate cancer based on proteomics

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Chinese Journal of Natural Medicines 2025年第1期23卷 64-76页

作者： Qiuping Zhang Qiuju Huang Zhiping Cheng Wei Xue Shoushi Liu Yunnuo Liao Xiaolan Li Xin Chen Yaoyao Han Dan Zhu Zhiheng Su Xin Yang Zhuo Luo Hongwei Guo Department of Traditional Chinese Medicine the First Affiliated Hospital of Guangxi Medical University Guangxi Key laboratory of Bioactive Molecules Research and Evaluation & College of Pharmacy Guangxi Medical University Key laboratory of Longevity and Aging-related Diseases of Chinese Ministry of Education & Center for Translational Medicine Guangxi Medical University

Xiaoaiping(XAP) Injection demonstrates the anti-prostate cancer(PCa) effects, yet the underlying mechanism remains unclear. This study aims to investigate the impact of XAP on PCa and elucidate its mechanism of action. PCa cell proliferation was evaluated using a cell counting kit-8(CCK-8) assay. Cell apoptosis was assessed through Hoechst staining and Western blotting assays. Proteomics technology was employed to identify key molecules and significant signaling pathways modulated by XAP in PCa cells. To further validate potential key genes and important pathways, a series of assays were conducted, including acridine orange(AO)staining, transmission electron microscopy, and immunofluorescence assays. The molecular mechanism of XAP against PCa in vivo was examined using a PC3 xenograft mouse model. Results demonstrated that XAP significantly inhibited cell proliferation in multiple PCa cell *** C4-2 and prostate cancer cell line-3(PC3) cells, XAP induced cellular apoptosis, evidenced by reduced B-cell lymphoma 2(Bcl-2) levels and elevated Bcl-2-associated X(Bax) levels. Proteomic, immunofluorescence, and quantitative reverse transcription-polymerase chain reaction(q RT-PCR) investigations revealed a strong correlation between forkhead box O3a(Fox O3a) autophagic degradation and the anti-PCa action of XAP. XAP hindered autophagy by reducing the expression levels of autophagy-related protein 5(Atg5)/autophagy-related protein 12(Atg12) and enhancing Fox O3a expression and nuclear translocation. Furthermore,XAP exhibited potent anti-PCa action in PC3 xenograft mice and triggered Fox O3a nuclear translocation in tumor tissue. These findings suggest that XAP induces PCa apoptosis via inhibition of Fox O3a autophagic degradation, potentially offering a novel perspective on XAP injection as an effective anticancer therapy for PCa.

关键词： Apoptosis Autophagy Forkhead box O3a Prostate cancer Xiaoaiping Injection

microRNAs: tiny RNA molecules, huge driving forces to move the cell

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Protein & Cell 2010年第10期1卷 916-926页

作者： Shenglin Huang Xianghuo He State Key laboratory of oncogenes and related genes Shanghai Cancer InstituteShanghai Jiao Tong University School of MedicineShanghai 200032China

Cell migration or movement is a highly dynamic cellular process,requiring precise regulation that is essential for a variety of biological ***(miRNAs)are a class of tiny non-coding RNA molecules that function as critical post-transcriptional regulators of gene *** evidence demonstrates that miRNAs play important roles in cell migration and directly contribute to extracellular matrix(ECM)remodeling,cell adhesion,and cell signalling that controls cell migration by targeting a large number of protein-coding ***,the dysregulation of these miRNAs has been linked to several migration-related *** this review,we summarize and highlight the recent advances concerning the roles and validated targets of miRNAs in the control of cell movement.

关键词： microRNA cell migration metastasis

A novel protein-DNA interaction involved with the CpG dinucleotide at -30 upstream is linked to the DNA methylation mediated transcription silencing of the MAGE-A1 gene

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Cell Research 2004年第4期14卷 283-294页

作者： Jie ZHANG, Jian YU, Jun GU, Bao Mei GAO, Ying Jun ZHAO, Peng WANG, Hong Yu ZHANG, Jing De ZHU The State-key laboratory for oncogenes and related genes, Shanghai Cancer Institute, Shanghai Jiao Tong University, LN 2200/25, Xietu Road, Shanghai 200032, China. 1The State-key laboratory for oncogenes and related genes Shanghai Cancer Institute Shanghai Jiao Tong University LN 2200/25 Xietu Road Shanghai 200032 China. 1The State-key laboratory for oncogenes and related genes Shanghai Cancer Institute Shanghai Jiao Tong University LN 2200/25 Xietu Road Shanghai 200032 China. 1The State-key laboratory for oncogenes and related genes Shanghai Cancer Institute Shanghai Jiao Tong University LN 2200/25 Xietu Road Shanghai 200032 China. 1The State-key laboratory for oncogenes and related genes Shanghai Cancer Institute Shanghai Jiao Tong University LN 2200/25 Xietu Road Shanghai 200032 China. 1The State-key laboratory for oncogenes and related genes Shanghai Cancer Institute Shanghai Jiao Tong University LN 2200/25 Xietu Road Shanghai 200032 China. 1The State-key laboratory for oncogenes and related genes Shanghai Cancer Institute Shanghai Jiao Tong University LN 2200/25 Xietu Road Shanghai 200032 China. 1The State-key laboratory for oncogenes and related genes Shanghai Cancer Institute Shanghai Jiao Tong University LN 2200/25 Xietu Road Shanghai 200032 China. 1The State-key laboratory for oncogenes and related genes Shanghai Cancer Institute Shanghai Jiao Tong University LN 2200/25 Xietu Road Shanghai 200032 China.

To understand the DNA-methylation mediated gene silencing mechanisms, we analyzed in cell culture of the promoter function of the MAGE-A1 gene, which is frequently demethylated and over-expressed in human hepatocellular carcinoma. We have established the correlation of the DNA methylation of the promoter CpG island with expression status of this gene in a panel of the established liver cancer cell lines. The crucial CpG dinucleotide（s） within the minimal promoter subjected to the control mediated by DNA methylation with profound biological functions was also delineated. Furthermore, a novel sequence-specific DNA-protein interaction at the -30 CpG dinucleotide upstream of the gene was found having a vital part to play in the DNA methylation mediated transcription silencing of the MAGE-A1 gene. Our results would not only provide new insights into the DNA methylation mediated mechanisms over transcription of the MAGE-A1 gene, but also pave the way for further defining the cross-talk among DNA methylation, h

关键词： MAGE-A1 DNA methylation transcriptional regulation.

ADAMTS12 promotes migration and epithelial-mesenchymal transition and predicts poor prognosis for pancreatic cancer

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Hepatobiliary & Pancreatic Diseases International 2023年第2期22卷 169-178页

作者： Rui-Zhe He Jia-Hao Zheng Hong-Fei Yao Da-Peng Xu Min-Wei Yang De-Jun Liu Yong-Wei Sun Yan-Miao Huo State Key laboratory of oncogenes and related genes Department of Biliary-Pancreatic SurgeryRenji HospitalShanghai Jiao Tong University School of MedicineShanghaiChina

Background: ADAMTS(a disintegrin and metalloproteinase with thrombospondin-like motifs) family, a group of extracellular multifunctional enzymes, has been proven to play a pivotal role in the tumor. In pancreatic cancer, the role and mechanism of this family remain unclear. The present study aimed to figure out the hub gene of ADAMTSs and explore the exact roles in the prognosis and biological functions in pancreatic ductal adenocarcinoma(PDAC). Methods: We used several databases to analyze the ADAMTS family and then screen out the hub genes. The expression of ADAMTS12 in 106 pairs of PDAC tumors and adjacent normal tissues was examined by immunohistochemistry, and its correlations with clinical parameters were further analyzed. The impacts of ADAMTS12 on the migration of PDAC cells were predicted by gene set enrichment analysis and confirmed by transwell assays. The potential impacts of ADAMTS12 on the epithelial-mesenchymal transition(EMT) were identified by database analysis and experimental proof of real-time quantitative polymerase chain reaction(q PCR) and Western blotting. Results: Our study found that ADAMTS12 was a crucial gene in PDAC, and it was highly expressed in tumor tissues when compared to that in the adjacent tissues. ADATMS12 had predictive value of a poor prognosis for PDAC. The elevation of ADAMTS12 was parallel to the progression of PDAC. Inhibition of ADAMTS12 suppressed the migration of PDAC cells and interfered with the process of EMT. Conclusions: ADAMTS12 is a crucial member of ADAMTSs in PDAC and a predictor of poor prognosis. Additionally, based on its impacts on migration and metastasis in PDAC and the relationship with EMT, ADAMTS12 plays a role of an oncogene in PDAC and may be a promising target for treatment.

关键词： ADAMTS12 Pancreatic ductal adenocarcinoma Prognosis Migration Epithelial-mesenchymal transition